Coactosin-like protein 1 inhibits neuronal migration during mouse corticogenesis
Guohong Li, Yupeng Yin, Jiong Chen, Yanle Fan, Juhong Ma, Yingxue Huang, Chen Chen, Pengxiu Dai, Shulin Chen, Shanting Zhao
Abstract
Guohong Li, Yupeng Yin, Jiong Chen, Yanle Fan, Juhong Ma, Yingxue Huang, Chen Chen, Pengxiu Dai, Shulin Chen, Shanting Zhao
Abstract
cells. Neuronal migration requires cytoskeletal remodeling and actin regulation. Although Cotl1 strongly binds to F-actin, the role of Cotl1 in neuronal migration remains undescribed. In this study, we revealed that Cotl1 overexpression impaired migrationof both early- and late-born neurons during mouse corticogenesis. Moreover, Cotl1 overexpression delayed, rather than blocked, neuronal migration in late-born neurons. Cotl1 expression disturbed the morphology of migrating neurons, lengthening the leading processes. This study is the first to investigate the function of Cotl1, and the results indicate that Cotl1 is involved in the regulation of neuronal migration and morphogenesis.
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cells. Neuronal migration requires cytoskeletal remodeling and actin regulation. Although Cotl1 strongly binds to F-actin, the role of Cotl1 in neuronal migration remains undescribed. In this study, we revealed that Cotl1 overexpression impaired migrationof both early- and late-born neurons during mouse corticogenesis. Moreover, Cotl1 overexpression delayed, rather than blocked, neuronal migration in late-born neurons. Cotl1 expression disturbed the morphology of migrating neurons, lengthening the leading processes. This study is the first to investigate the function of Cotl1, and the results indicate that Cotl1 is involved in the regulation of neuronal migration and morphogenesis.
Key concepts: Corticogenesis, Neuronal migration, Cofilin, Cell biology, Biology, Cytoskeleton, Dictyostelium discoideum, Actin